Potassium Regulation

Potassium interpretation starts with three questions: Is the result credible? Is the patient electrically or neuromuscularly unstable? Is the abnormality caused by a change in total-body potassium, a shift between compartments, or both? Serum or plasma potassium samples only the extracellular compartment. A rapid shift can therefore produce a dangerous concentration without proving a large total-body surplus, while a depleted patient may transiently show a less abnormal serum value. Potassium helps set the resting membrane potential of cardiac, skeletal-muscle, and nerve cells. Insulin and beta-adrenergic activity promote movement into cells. Acidosis, tissue injury, insulin deficiency, and some medicines can move potassium out of cells. The kidneys provide the main route of sustained potassium removal; distal sodium delivery, tubular flow, and aldosterone influence urinary secretion. Gastrointestinal losses, renal losses, inadequate intake, or intracellular shifting can lower the measured concentration. Reduced kidney clearance, cellular release, impaired aldosterone effect, or potassium intake that exceeds excretion can raise it. This explains why temporizing and definitive treatments are different. Insulin with glucose and salbutamol redistribute potassium into cells but do not remove it from the...